Diabetes mellitus has serious effects on people's health and accompanies various complications. There are two major types of diabetes mellitus: type I diabetes mellitus characterized by little or no insulin secretory capacity due to the destruction of pancreatic cells, and type II diabetes mellitus characterized by insulin deficiency and insulin resistance due to other causes. The prevalence of type II diabetes mellitus is 90% or more of total patients with diabetes mellitus. Representative examples of complications accompanying diabetes include hyperlipidemia, hypertension, retinopathy and renal insufficiency (Paul Zimmer, et al., Nature, 2001, 414, 782). Sulfonylureas (stimulating insulin secretion in pancreatic cells), biguanides (inhibiting glucose production in the liver), α-glucosidase inhibitors (inhibiting glucose absorption in the intestines), etc. have been used as agents to treat diabetes. Recently, peroxisome proliferator-activated receptor gamma (PPARγ) accelerators (Thiazolidinediones, increasing insulin sensitivity) have drawn attention as therapeutic agents for diabetes. However, these drugs have side effects such as hypoglycemia, weight gain and the like (David E. Moller, Nature, 2001, 414, 821). Accordingly, there is a strong need to developed diabetes therapeutic agents with decreased side effects, in particular without inducing hypoglycemia and weight gain.
Recently, it has been found that dipeptidyl peptidase-IV (DPP-IV) deficient mice maintained glucagon-like protein 1 (GLP-1) activity and high insulin levels, resulting in decreased blood glucose levels, which suggested the possibility of it being used as a therapeutic agent for diabetes (Marguet D. et al, Natl. Acad. Sci. USA, (2000) 97, 6874-6879). GLP-1 induces differentiation and growth of pancreatic β-cells in vivo and plays an important role in the production and secretion of insulin. GLP-1 is inactivated by DPP-IV, and DPP-IV inhibitors have been reported to increase insulin secretion by means of inhibiting said inactivation mechanism. DPP-IV inhibitors are also being developed as a treatment for obesity because they lead to satiety in rats and slow down digestion of foods in the intestines, resulting in weight loss. Further, many investigators have also shown that DPP-IV inhibitors control blood glucose and lipid levels in animal experiments (Pospislik J. A., et al, Diabetes, (2002) 51, 943-950). In this regard, DPP-IV inhibitors can be considered as potentially useful agents for treatment of diabetes.
To date, much research for developing DPP-IV inhibitors has focused on materials in which cyano group is bonded to pyrrolidine ring. For example, WO 00/34241 discloses DPP-IV inhibitors represented by the below formula.

wherein R is an adamantyl group, and n is 0 to 3.
Another inhibitors are disclosed in WO 04/064778, WO 03/004498, WO 03/082817, etc., and among them, WO 04/064778 discloses DPP-IV inhibitors represented by the below formula.

wherein Ar is unsubstituted or substituted phenyl group; R15, R16 and R17 are hydrogen or alkyl group; and U, V and W are nitrogen, oxygen, or substituted nitrogen or carbon.
WO 03/004498 discloses DPP-IV inhibitors represented by the below formula.

wherein Ar is unsubstituted or substituted phenyl group; R18 is hydrogen or alkyl group; and T is nitrogen or substituted carbon.
WO 03/082817 discloses DPP-IV inhibitors represented by the below formula.

wherein Ar is unsubstituted or substituted phenyl group; R19, R20 and R21 are hydrogen or alkyl group; and Q is nitrogen or substituted carbon.
These DPP-IV inhibitors has the amide bond in their molecular structures likewise the present invention; however, the unsubstituted or substituted phenyl groups which is represented as Ar in the above formulas of these inhibitors are entirely different from the saturated or unsaturated, 5-membered or 6-membered heterocyclic substituents of the present invention. Moreover, DPP-IV inhibitors of the present invention having the lactam ring at the phenyl group position of the above inhibitors have not been disclosed in the prior art.